CARDIOVASCULAR7 Nov 2020

REFERENCE

• BRAUNWAULD

• ESC GUIDELINES

• AHA GUIDELINES

1. A 64-year-old woman presents to the emergency department with nausea and vomitting. Her ECG shows ST-segment depression in the inferior leads and the serum troponin T is elevated. Each of the following statements regarding acute coronary syndrome (ACS) in women is true EXCEPT

A. Women are more likely to develop symptoms of angina than to present initially with a myocardial infarction (MI)

B. Women tend to be older than men at the time of presentation

C. In the setting of an MI, women are more likely than men are to present with nausea, palpitations, shortness of breath, and neck, jaw, and back pain

D. Women have a higher prevalence of vasospastic and microvascular angina than men

E. Women <50 years of age have lower mortality rates during ACS than men of the same age

E. Women <50 years of age have lower mortality rates during ACS than men of the same age

• It had long been thought that men and women had similar clinical presentations of CAD, but evidence now shows otherwise. Women are more likely to develop angina as the first manifestation of heart disease and less likely to present with an acute myocardial infarction than men. Women also tend to be, on average, 5 to 10 years older than men at the time of symptom onset. Women presenting with an MI are more likely to experience nausea, shortness of breath, palpitations, and neck, jaw, and back pain and are less likely to experience diaphoresis. It is not clear what accounts for these differences. Perhaps the age at presentation results in a higher incidence of comorbid conditions such as diabetes, hypertension, and congestive heart failure. Angiographic findings are similar, but women have a higher prevalence of vasospastic and microvascular angina. Mortality rates appear to differ between men and women as well, with women <50 years of age having a twofold greater mortality in association with acute MI.

2. Physiologic states and dynamic maneuvers alter the characteristics of heart murmurs. Which of the following statements is correct?A. In acute mitral regurgitation, the left atrial pressure rises dramatically so that the murmur is heard only during late systoleB. Rising from a squatting to a standing position causes the murmur of mitral valve prolapse to begin later in systole C. The diastolic rumble of mitral stenosis becomes more prominent during the strain phase of a Valsalva maneuverD. The murmur of aortic stenosis, but not mitral regurgitation, becomes louder during the beat after a premature ventricular contractionE. The murmur of acute aortic regurgitation can usually be heard throughout diastole

The intensity of a heart murmur pressure gradient and rate of flow across the responsible orifice. Physiologic changes or bedside maneuvers that alter the driving pressure gradient or the rate of flow lead to audible changes in murmur intensity. In acute mitral regurgitation (MR), flow is directed backward from the left ventricle into a relatively noncompliant left atrium, leading to a rapid increase in left atrial pressure during systole. Because this abolishes the pressure gradient between the left ventricle and left atrium in late systole, the murmur of acute MR is often present only in early systole. Similarly, in acute aortic regurgitation, the left ventricular (LV) diastolic pressure rises rapidly, leading to cessation of the diastolic murmur in mid to late diastole, as LV and aortic pressures equalize.

D. The murmur of aortic stenosis, but not mitral regurgitation, becomes louder during the beat after a premature ventricular contractionIn patients with mitral valve prolapse, the auscultatory findings vary prominently with physiologic alterations. The valve physically prolapses into the left atrium, and the associated click/murmur commences when the reduction of LV volume during contraction reaches the point at which the mitral leaflets fail to coapt. Maneuvers that decrease LV volume, such as standing from a squatting position, cause the valve prolapse, the click, and the murmur to all occur earlier in systole. In mitral stenosis, the diastolic rumbling murmur increases with any maneuver that augments transvalvular flow and decreases in situations that reduce transmitral flow, such as the strain phase of the Valsalva maneuver. The systolic murmurs of aortic valvular stenosis and MR are sometimes difficult to distinguish. However, the intensity of aortic stenosis varies from beat to beat when the duration of diastole is not constant, as in atrial fibrillation or after a premature contraction. The murmur of MR is not affected in this manner, because the changes in driving pressure between the left ventricle and the left atrium are smaller.

3. Each of the following statements about myocardial contraction is true EXCEPT

A. Beta1-adrenergic stimulation increases the concentration of intracellular calcium

B. Beta1-adrenergic stimulation promotes production of intracellular cyclic guanosine monophosphate

C. Interaction of calcium with troponin C is essential for myocytecontraction

D. Myosin molecules are tethered to the Z line by the protein titin

E. The sarcoplasmic reticulum plays a key role in the release and uptake of calcium

B. Beta1-adrenergic stimulation promotes production of intracellular cyclic guanosinemonophosphate• The beta1 receptor is coupled, via G-proteins, to activation of adenylate cyclase

and formation of cyclic adenosine monophosphate (cAMP). The rise in cytosolic calcium increases calcium–troponin C interaction, a necessary step for subsequent contraction. The activated troponin C binds tightly to the inhibitory molecule troponin I, thus removing inhibition of actin-myosin cross-bridge formation, and contraction ensues. Whereas cAMP is a second messenger for the betaadrenergic system, another cyclic nucleotide, cyclic guanosinemonophosphate (cGMP), acts as a second messenger during cholinergic stimulation. In vascular smooth muscle, cGMP acts as an intracellular messenger after nitric oxide stimulation. Titin is a large protein that provides elasticity and supports the myosin molecule by tethering it to the myocyte Z line.

4. Which of the following statements regarding the auscultatoryfindings of mitral stenosis is correct?

A. The opening snap (OS) is a late diastolic sound

B. A long A2-OS interval implies severe mitral stenosis

C. In atrial fibrillation, the A2-OS interval does not vary with cycle length

D. The “snap” is generated by rapid reversal of the position of the posterior mitral leaflet

E. The presence of an opening snap implies a mobile body of the anterior mitral leaflet

E. The presence of an opening snap implies a mobile body of the anterior mitral leaflet

• In mitral stenosis, the opening snap is an early diastolic sound generated when superior systolic bowing of the anterior mitral valve leaflet is rapidly reversed toward the left ventricle in early diastole, as a result of the high left atrial pressure. The presence of an opening snap implies a mobile body of the anterior mitral leaflet. The timing of the A2-OS interval relates to the severity of mitral stenosis. When mitral stenosis is advanced and left atrial pressure is therefore high, left atrial and left ventricular pressures equilibrate earlier in diastole, resulting in a shorter A2-OS interval. This interval varies in atrial fibrillation according to the previous cycle length. During relatively short cycles, left atrial pressure is higher (because less atrial emptying can occur) and the A2-OS interval lessens.

5. A 36-year-old man from the Dominician Republic presents to the emergency department with shortness of breath. A grade III/IV systolic murmur is auscultated at the apex. The chest radiograph demonstrates pulmonary vascular congestion. Echocardiography in emergency department confirms the presence of mitral regurgitation and vigorous left venticular contractile function. Which of the following findings would suggest the acute onset of mitral regurgitation?

A. Presence of cardiomegaly on the chest radiograph

B. Left atrial and ventricular hypertrophy on the ECG

C. The systolic murmur is short and ends prior to S2

D. Normal jugular venous pressure

C. The systolic murmur is short and ends prior to S2

• In acute MR the ECG is usually normal, while in chronic MR abnormalities such as P mitrale, atrial fibrillation, and LV hypertrophy are frequently present. The heart size is usually normal in acute MR; cardiomegaly and left atrial enlargement are prominent in chronic MR. While the murmur frequently radiates to the axilla in chronic MR, it can radiate to the neck, spine, and top of the head in acute MR, depending on the location of the jet. Furthermore, in patients with acute MR who have a normal-sized left atrium, the left atrial pressure rises abruptly, frequently leading to pulmonary edema and elevated jugular venous pressure (JVP). The murmur may not be holosystolic but instead may be decrescendo, ending well before A2. It is also usually lower pitched and softer than the murmur of chronic MR.

6. Which of the following statements about the clinical findings in patients with atrial septal defects (ASD) is NOT correct?

A. A midsystolic ejection murmur and a diastolic rumbling murmur at the lower left sternal border are common features on cardiac exmination

B. Patients with ostium primum defects usually show right ventricular hypertrophy, a small rSR’ pattern in the right precordial levels, and rightward axis on the ECG

C. Tall R or R’ waves in V1 may signal the development of pulmonary hypertension

D. Echocardiographic features of ASD include right venticular and pulmonary arterial dilatation and paradoxical intraventricular septal motion

E. Radiographic features include cardiomegaly, dilatated central pulmonary arteries, and pulmonary plethora

B. Patients with ostium primum defects usually show right ventricular hypertrophy, a small rSR’ pattern in the right precordial levels, and rightward axis on the ECG• a midsystolic pulmonary ejection murmur due to increased flow across the pulmonic valve. If

the shunt is large, a middiastolic rumbling murmur may be audible at the lower left sternal border. This murmur results from increased blood flow across the tricuspid valve. The ECG in ostium secundum ASD usually shows right-axis deviation and an rSR′ or rsR′ pattern in the right precordial leads with a normal QRS complex duration. Left-axis deviation and superior orientation of the QRS complex in the frontal plane is consistent with either an ostium primumdefect or, less commonly, a secundum atrial defect combined with mitral valve prolapse. Tall R or R′ waves in V1 may indicate the presence of pulmonary hypertension and concomitant RV hypertrophy. The chest radiograph may reveal enlargement of the right atrium and right ventricle, pulmonary arterial dilatation, and increased pulmonary vascular markings. Echocardiographic evaluation of ASD commonly shows pulmonary arterial and RV dilatation as well as anterior systolic (paradoxical) intraventricular septal motion, reflecting RV volume overload.

7. A 36-year-old woman with no prior history of cardiac disease develops exertional dyspnea and orthopnea 1 month after delivering a healthy full-term infant. Echocardiography demonstrates a dilatated left ventricle with globally reduced contractile function. Which of the following statement regarding peripartum cardiomyopathy (PPCM) is correct?A. Symptoms of PPCM always arise during the last month of pregnancy or

within 1 week after deliveryB. Clinical and hemodynamic findings in PPCM are indistinguishable from

those of other forms of dilatated cardiomyopathyC. The incidence of PPCM is greatest in first pregnanciesD. Approximately 10% of PPCM patients show recovery within the first 6

months after deliveryE. Younger maternal age is a risk factor for PPCM

b. Clinical and hemodynamic findings in PPCM are indistinguishable from those of other forms of dilatatedcardiomyopathy• Peripartum cardiomyopathy (PPCM) is a form of dilated cardiomyopathy that occurs for the first

time in the antepartum or postpartum period and is clinically indistinguishable from other types of dilated cardiomyopathy. It is generally defined by four criteria: (1) the development of cardiac failure in the last month of pregnancy or within 5 months of delivery, (2) absence of an identifiable cause for the cardiac failure, (3) absence of recognizable heart disease before the last month of pregnancy, and (4) left ventricular systolic dysfunction demonstrated by classic imaging criteria. The incidence of PPCM is approximately 1 in 3000 pregnancies, and risk factors for its occurrence include multiparity, being black, older maternal age, and preeclampsia. Approximately 50% of patients with PPCM show complete or near-complete recovery during the first 6 months after delivery. Subsequent pregnancies in patients with PPCM with persistent cardiac dysfunction should be discouraged because of the high likelihood of relapse. Even patients who have recovered from an episode of PPCM have a 30% risk of experiencing relapse during subsequent pregnancies.

8. Each of the following statement regarding hemodynamic changes during normal pregnancy is correct EXCEPT

A. Total blood volume increases

B. Cardiac output increases

C. Stroke volume increases

D. Heart rate increases

E. Systemic vascular resistance increases

e. Systemic vascular resistance increases

9. Which of the following statements about peripheral edema in heart failure is correct, except?

A. Edema in heart failure is not correlates with the level of systemic venous pressure

B. Peripheral edema may be detected when extracellular fluid volume has increased by as little as 1 to 2 liters

C. Rupture of the skin with extravasation of fluid is more likely to occur with sudden volume overload than with chronic development of edema

D. In patients with hemiplegia due to a cerebrovascular accident, edema is usually more apparent on the paralyzed side

B. Peripheral edema may be detected when extracellular fluid volume has increased by as little as 1 to 2 liters

Although peripheral edema is a common and important physical finding in congestive heart failure, its presence does not correlate well with the level of systemic venous pressure. The excess volume of extracellular fluid is a more important determinant of edema. In adults, a minimum of 4 liters of excess extracellular fluid volume usually must accumulate before peripheral edema is manifested. In patients with chronic left ventricular failure and a low cardiac output, peripheral edema may develop in the presence of normal or minimally elevated systemic venous pressure because of a gradual but persistent accumulation of extracellular fluid volume. Edema generally accumulates in dependent portions of the body such as the ankles or feet of ambulatory patients or the sacrum of bedridden patients. In rare instances, especially when edema develops suddenly and severely, frank rupture of the skin with extravasation of fluid may result. Edema is usually more marked on the paralyzed side of patients with hemiplegia; unilateral edema may also result from unilateral venous obstruction.

10. A murmur is auscultated during routine examination of an 18-year-old asymptomatic college student, at the second left intercostal space, closure to the sternum. The murmur is crescendo-decrescendo, is present through-out systole and diastole, and peaks simultaneously with S2. It does not change with position or rotation of the head. Which of the following best describes this murmur?

A. This is continous murmur, most likely a venous hum commonly heard in adolescents

B. This is a continous murmur resulting from mixed aortic valve disease

C. This is a continous murmur due to a congenital shunt, likely a patent ductusarteriosus

D. Continous murmurs of this type can only be congenital; murmurs due to acquired arteriovenous connections are purely systolic

E. This murmur, the result of left subclavian artery stenosis, is not considered continous, because a continous murmur can result only from an arteriovenouscommunication

c. This is a continous murmur due to a congenital shunt, likely a patent ductus arteriosus

• The term continuous applies to murmurs that begin in systole and continue without interruption into part or all of diastole. The murmur described here, that of a patent ductusarteriosus, is the classic continuous murmur, peaking in intensity just before or after S2 then decreasing in intensity during diastole. Continuous murmurs may be congenital or acquired and can be caused by (1) an aortopulmonary shunt, such as patent ductus arteriosus; (2) an arteriovenous shunt, including arteriovenous fistulas, coronary artery fistulas, or rupture of an aortic sinus of Valsalva aneurysm into a right heart chamber; (3) constricted arterial vessels (e.g., a femoral arterial atherosclerotic stenosis); (4) turbulence in nonconstricted arteries (e.g., the “mammary souffle,” an innocent flow murmur heard during late pregnancy and the puerperium over the lactating breast and augmented by light pressure with the stethoscope); or (5) venous murmurs, such as a cervical venous hum, an often “rough” sounding murmur present in healthy children and young adults. The cervical hum may be accentuated by deforming the internal jugular vein with rotation of the head. It is augmented during pregnancy and in disease states in which there is increased venous flow, such as thyrotoxicosis. The combined murmurs of aortic stenosis and regurgitation have distinct systolic and diastolic components and do not constitute a continuous murmur.

11. A 68-year-old man presents to a non-PCI facility with anterior STEMI with ST elevation from V2 to V5. He is short of breath with bilateral rales. Chest pain started 4 h earlier. He had a TIA 6 weeks earlier and is on clopidogrel and statin. Estimated transport time to nearest catheterization laboratory is 75 min. After giving O2, nitroglycerin (NTG), ASA, and heparin, what is the best next strategy?

A. Immediate transfer to the PCI facility

B. Give half-dose thrombolytic and then transfer

C. Patient is too high risk to transfer; give full-dose thrombolytic

D. None of the above

a. Immediate transfer to the PCI facility

12. Of the following statements regarding a patient with multiple cardiac risk factors and angina-like chest pain lasting 30 min, which is the incorrect one?

A. A normal echocardiogram (ECG) in the emergency room (ER) rules out myocardial infarction (MI)

B. Ischemia in circumflex area is more often electrically silent

C. Negative first set of cardiac markers does not rules out MI

D. ECG changes could be dynamic, and it is useful to repeat every 15 min in the first hour of chest pain or when chest pain recurs

A. A normal echocardiogram (ECG) in the emergency room (ER) rules out myocardial infarction (MI)

13. Which of the following types of chest pain rule in ACS?A. Sharp stabbing chest pain

B. Pleuritic chest pain

C. Chest pain reproduced by palpation

D. None of the above

d. None of the above

14. The GRACE risk model predicts in hospital mortality in ACS patients and includes Killip class, systolic blood pressure (BP), heart rate, age, and serum creatinine level. Which one of the following may be negatively correlated with mortality?

A. Heart rate

B. Systolic BP

C. Killip class

D. None of the above

b. Systolic BP

15. Regarding use of traditional nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX-2) inhibitors in the setting of ACS, which of the following statements is correct?

A. Traditional NSAIDs, but not COX-2 inhibitors can be used

B. Traditional NSAIDs should be used, but COX-2 inhibitors can be used

C. Neither traditional NSAIDs nor COX-2 inhibitors should be used

D. Either can be used with no risk of harm

c. Neither traditional NSAIDs nor COX-2 inhibitors should be used

16. Which calcium channel blockers are contraindicated in ACS?A. Diltiazem

B. Verapamil

C. Short-acting nifedipine without a beta blocker

D. None of the above

c. Short-acting nifedipine without a beta blocker

17. A 64-year-old man presents to a non-PCI facility with anterior STEMI with ST elevation from V2 to V4. He is short of breath with bilateral rales. Chest pain started 3 h earlier. He is on aspirin and statin. Estimated transport time to nearest catheterization laboratory is 4 h. There are no contraindications for thrombolytic therapy. After giving O2 ,NTG, ASA chewed,and heparin,what is the best next strategy?

A. Full-dose thrombolytic and transfer to PCI facility

B. Half-dose thrombolytic and transfer to PCI facility

C. Immediately transfer to PCI facility

D. Treat medically as the patient is high risk to transfer

a. Full-dose thrombolytic and transfer to PCI facility

18. Aspirin in suspected ACS is avoided in which of the following patients?

A. Aspirin allergy

B. Recent gastrointestinal bleed

C. Neither A nor B

D. Both A and B

d. Both A and B

19. For patients with ACS, what is the recommended duration of double antiplatelet therapy (DAPT)?

A. 1month

B. 6months

C. 1year

D. Forever, unless at high risk of bleeding

c. 1year

20. Which of the following should not be used as the sole anticoagulant during PCI?

A. Fondaparinux

B. Enoxaparin

C. Bivalirudin

D. None of the above

a. Fondaparinux

21. Which of the following statements are accurate the duration of stoppage of antiplatelet drugs before elective coronary artery bypass grafting?

A. Clopidogrel for 5 days

B. Prasugrel for 7 days

C. Eptifibatide and tirofiban for 2–4 h

D. Abciximab for 12 h

E. All of the above

d. All of the above

22. Which of the following statements are accurate regarding triple antithrombotic therapy after MI?

A. The duration should be minimized

B. Concomitant proton pump inhibitors should be used

C. Triple therapy should not be used

D. A and B are correct

d. A and B are correct

23. Which of the following agents are useful for secondary prevention post MI?

A. Vitamin E

B. Folic acid

C. Beta carotene

D. Fish oil

E. None of the above

e. None of the above

24. In ACS due to cocaine use, it is preferable to avoid which of these agents?

A. Heparin

B. Beta blocker

C. ACEI

D. None of the above

b. Beta blocker

• The dominant underlying pathophysiologic factor in cocaine-induced ACS can be coronary spasm or thrombus formation caused by α-adrenergic stimulation. Atherosclerosis is also accelerated by cocaine use. This patient should be started on aspirin, sublingual nitroglycerin, and intravenous heparin. β-Blockers are contraindicated as they may allow unopposed β-adrenergic stimulation and have been associated with increased mortality.

25. For a patient presenting with STEMI to a non-PCI facility, which of the following factors support immediate thrombolytic therapy?

A. Presentation within 4 h of chest pain

B. Low-risk STEMI

C. Low bleeding risk with thrombolysis

D. PCI facility is far away

E. All of the above

e. All of the above

• Thanks